IngredientsD-tagatose is a six-carbon monosaccharide ketohexose carbohydrate. Synonyms include tagatose, D-lyxo-hexulose, and Ξ±-D-tagatose; it is often referred to as a rare sugar. It is a C-4 epimer of D-fructose and an isomer of D-galactose; it is water soluble and of a white or almost white crystalline structure. The IUPAC name is (3S,4S,5R)-2-(hydroxymethyl)oxane-2,3,4,5-tetrol. Its molecular formula is C6H12O6 with a molecular weight of 180 g/mol.
Chemically, tagatose is a ketose. The only structural difference between tagatose and fructose is the reversed orientation of the hydroxyl group on the fourth carbon. D-tagatose, with the molecular formula C6H12O6, is the ketose form of D-galactose and the epimer of D-fructose at the C-4 position.
Tagatose has a clean, neutral sweet taste. It is a white, odorless, crystalline powder, well soluble in water (approximately 160 g/100 mL at 20Β°C) and poorly soluble in ethanol, with low hygroscopicity β it does not readily attract moisture. Its melting point is 133β137Β°C. Tagatose is a reducing sugar, which undergoes the Maillard browning reaction with amino acids, so it gives a brown color to baked goods.
Tagatose is a monosaccharide naturally found in small amounts in some fruits and dairy products. It is a rare natural carbohydrate found in some fruits (apples, oranges, and pineapple) and sterilized milk at levels ranging from 1 to 3.5 g/kg. Tagatose is found in trace quantities in various natural foods, including sterilized powdered milk, hot cocoa, cheese, yogurts, and other dairy products. Breast milk has also been identified as a source of tagatose, and tagatose occurs naturally at low levels in the gum from Sterculia setigera (an evergreen tree).
As a food ingredient, tagatose must be synthesized due to economic constraints associated with extracting its low quantities from natural sources. Tagatose can be produced through either chemical synthesis or enzymatic methods. Tagatose can be produced for the commercial market using lactose, fructose, or maltodextrin as feedstocks, as well as by enzymatic conversion of starches.
Tagatose is a bulk sweetener with no odor or off-flavors. It is a white crystalline powder that takes part in the Maillard reaction, which leads to the browning of food. As a food additive, tagatose can be used as a sweetener, texturizer, stabilizer, humectant, formulation aid, and, being a highly Maillard reactive reducing sugar, it can be used as a flavoring agent. In its commercial form, tagatose is used in beverages, yogurt, chewing gum, chocolate, baked goods, and dietary supplement formulations.
According to the available literature on carbohydrate chemistry, D-tagatose was discovered by Lobry de Bruyn and Van Ekenstein in 1897, while experimenting on the effects of mild alkali on D-galactose. They noticed that aldoses changed into epimeric aldoses in addition to one or more corresponding 2-ketoses; the additional molecule was named tagatose.
In 1939, Yvonne and coworkers succeeded in the alkaline conversion of D-galactose into a crystalline product and named it Ξ±-D-tagatose. Its natural occurrence was confirmed in 1949 when E. L. Hirst, L. Hough, and J. K. N. Jones isolated D-tagatose from the acid hydrolysate of gum exudates from the tropical tree Sterculia setigera using paper partition chromatography, highlighting its presence as a minor component in plant exudates.
Tagatose, a sugar that appears in nature in small quantities, began its unusual journey to the commercial market nearly 30 years ago, when Dr. Gilbert V. Levin invented a life detection experiment to place aboard NASA's Mars Viking 1 and Viking 2 landers. D-tagatose was subsequently proposed as a sweetener by Gilbert Levin, after unsuccessful attempts to market L-glucose for that application. He patented an inexpensive method to make tagatose in 1988.
Tagatose was initially synthesized economically by isomerization of galactose derived from inexpensive whey powder using calcium catalysts, in a process patented in 1992. Biospherics Incorporated developed and filed a patent (US5356879A) for D-tagatose in 1992, which they licensed to MD Foods in 1997. MD Foods later merged with the Danish-Swedish multinational cooperative Arla Foods in 2001.
Unlike many botanical dietary supplements, D-tagatose has no documented history of deliberate traditional or ethnomedicinal use. Because it occurs only in trace amounts within dairy products, gum exudates, and certain fruits, human populations would have consumed it only incidentally as part of their ordinary diet rather than as a targeted preparation. There is no documented record of any culture deliberately isolating or using tagatose for medicinal purposes prior to its scientific identification in the nineteenth century. Its history as an intentional dietary ingredient begins with the synthetic and enzymatic manufacturing methods developed in the late 20th century.
In 2001, the Food and Drug Administration (FDA) recognized tagatose as Generally Recognized As Safe (GRAS). This designation means that scientific evidence supports the intended use of tagatose as a sugar substitute. The United States Food and Drug Administration approved tagatose as a food additive in October 2003. The Korea Food and Drug Administration approved tagatose as a health functional food for its antihyperglycemic effect. The European Food Safety Authority approved tagatose as a novel food and novel food ingredient. New Zealand and Australia have also approved tagatose for human consumption.
In the EU, the EFSA approved D-tagatose as a novel food ingredient, to be used without limit in all foods except infant formula. In Canada, D-tagatose is licensed as a Natural Health Product. Neither FDA, EFSA, nor Health Canada have defined an upper limit for D-tagatose consumption, and JECFA ruled in 2006 that D-tagatose had an ADI that was "not specified," a designation given to only the safest foods, meaning that no level tested thus far has been deemed unsafe.
In 2011, the European Food Safety Authority (EFSA) Panel on Dietetic Products, Nutrition and Allergies (NDA) issued a scientific opinion on the substantiation of health claims related to sugar replacers including tagatose, and maintenance of tooth mineralization by decreasing tooth demineralization and reduction of post-prandial glycemic responses. The US FDA has affirmed tagatose as GRAS since 2001, and has authorized a health claim for tagatose supporting its role in the reduction of dental caries.
Only 15β20% of D-tagatose is absorbed in the small intestine, leaving the remaining 80β85% of ingested D-tagatose to be fermented in the colon by indigenous microflora, leading to various prebiotic effects and a reduced caloric value compared to traditional sugars. Radio-labeling showed that approximately 20% is passively absorbed by diffusion, and this portion is metabolized in the liver like fructose. Tagatose provides only 1.5 calories (kilocalories) per gram according to food labels in the United States, or 2.4 kcal/g according to food labels in the European Union, so it is considered a low-calorie sweetener.
In the human liver, tagatose is metabolized the same way as fructose β it is converted to glucose, which can then either be stored in the form of glycogen or broken down to produce energy. While both fructose and tagatose are transformed to 1-phosphates in the liver, the rate of cleavage of the tagatose phosphate is only approximately 10% of the rate of cleavage of the fructose phosphate, resulting in partial excretion of unmetabolized tagatose β estimated at approximately 20% of the absorbed amount, or 5% of the ingested quantity.
D-tagatose is phosphorylated to tagatose-1-phosphate by fructokinase. Its slower rate of breakdown results in the accumulation of tagatose-1-phosphate, which stimulates glucokinase and promotes the conversion of glucose to glucose-6-phosphate. Glucose-6-phosphate in turn stimulates liver glycogen synthase to accelerate glycogen formation. It has also been proposed that D-tagatose directly inhibits the absorption of glucose by intestinal disaccharidases. Another proposed hypothesis is the inhibition of hepatic glycogenolysis; tagatose appears to act by promoting glycogen synthesis and decreasing glycogen utilization.
Due to poor absorption, tagatose has a minimal effect on blood glucose and insulin levels, resulting in a low glycemic index (GI). The GI for tagatose is reported to be around 3, which is significantly lower than the GI of sucrose (approximately 65).
It has been hypothesized that undigested tagatose reaches the colon and is fermented by colonic bacteria, resulting in the production of short-chain fatty acids (SCFA) which stimulate GLP-1 secretion from colonic L-cells, which in turn improves glycemic control by increasing insulin sensitivity and insulin secretion. Tagatose is selectively fermented by beneficial microbes such as Bifidobacterium and Lactobacillus, producing short-chain fatty acids (SCFAs).
There are reports that D-tagatose can exert antioxidant action through the elimination of free radicals, thus reducing cellular oxidative stress. It can also be observed that D-tagatose has an antioxidant action, favoring the elimination of free radicals and, consequently, causing a reduction in cellular oxidative stress.
Tagatose has been shown to reverse bacterial coaggregations, including periodontopathogen species, and to impair the activity and growth of the cariogenic bacterium S. mutans. Additionally, tagatose inhibits biofilm formation, pH decrease, and insoluble glucan synthesis in S. mutans.
Different clinical trials conducted in both healthy subjects and diabetic patients confirm the ability of D-tagatose to decrease postprandial blood glucose rise and reduce glycosylated hemoglobin (HbA1c).
Early human studies suggested tagatose as a potential antidiabetic drug through its beneficial effects on postprandial hyperglycemia and hyperinsulinemia. Consuming tagatose significantly blunted the rise in plasma glucose levels after oral glucose intake in patients with diabetes mellitus, without significantly affecting insulin levels (Donner et al., 1999).
A randomized study evaluated the safety and effect of D-tagatose on glycemic control in patients with type 2 diabetes at the end of 6 months with different doses β 2.5 g, 5.0 g, or 7.5 g three times per day β with basal glycemia dropping in the 3- and 6-month assessments only in the group that received a dose of 7.5 g. A Phase 2 study conducted by Ensor et al. (2014) determined that the lowest dose of D-tagatose capable of lowering HbA1c is 5.0 g taken three times a day.
A Phase 3 clinical trial with D-tagatose demonstrated statistically significant reductions in hemoglobin A1c (HbA1c) levels in patients with mild type 2 diabetes. Type 2 diabetic patients not taking any blood glucose-lowering medications were administered either 15 g of D-tagatose dissolved in 125β250 mL of water three times a day or placebo with meals. Reduction in HbA1c was statistically significant compared to placebo at all post-baseline time points in the intent-to-treat (ITT) population. Additionally, secondary endpoints were achieved in the ITT population with regard to LDL, total cholesterol, fasting blood glucose, and proportion of subjects achieving HbA1c targets of <7%. D-tagatose was effective at lowering HbA1c levels when administered at a daily dose of 15 g in 125β250 mL of water three times per day just prior to meals. The longer a patient was on D-tagatose therapy in compliance with instructions, the better the efficacy.
A systematic review and meta-analysis found that small doses (β€10 g/meal) of fructose and its low-caloric epimers β including tagatose β decrease the glycemic response to high glycemic index meals. Small doses of tagatose significantly reduced HbA1c (MD = β0.20%; 95% CI: β0.34%, β0.06%) and fasting glucose (MD = β0.30 mmol/L; 95% CI: β0.57 mmol/L, β0.04 mmol/L) without affecting fasting insulin. The certainty of the evidence of the effect of tagatose on HbA1c, fasting glucose, and fasting insulin was graded as moderate.
A more recent systematic review and meta-analysis searched the Medline, Embase, and Cochrane libraries through April 30, 2025, for controlled human intervention trials. Of 4,905 initial reports, 20 trials were identified, including 8 tagatose trials comprising 1,033 participants. A separate systematic review conducted by Noronha et al. (2018) found moderate evidence for the effects of administering small doses of fructose and tagatose (10 g) on the reduction of HbA1c and fasting glycemia, emphasizing that future long-term clinical trials will be essential to better support these estimates.
Strength of evidence summary: The fermentation of tagatose and subsequent effects on glycemic control have only been demonstrated in preclinical models, with limited clinical trials examining the effect of tagatose on glycemic control. The overall evidence for postprandial glucose reduction is moderate; evidence for long-term HbA1c control in type 2 diabetes is promising but derives primarily from small or industry-associated trials, and further independent replication is needed.
In two studies in patients with type 2 diabetes, both Donner et al. (8 participants) and Ensor et al. (112 participants) demonstrated that the ingestion of D-tagatose resulted in weight loss in a dose- and time-dependent manner. Specifically, Donner et al. showed that 45 g/day of D-tagatose for 12 months led to a mean reduction of 3.1 kg in an uncontrolled trial, while Ensor et al. confirmed this effect with a mean reduction of 5.1 kg in body weight with 45 g/day of D-tagatose for 12 months in a randomized controlled parallel trial.
No adverse metabolic or biochemical effects were noted among the 8 subjects who completed the 12-month pilot study. Significant and beneficial changes were seen in weight and HDL cholesterol at the end of the 12-month intervention period, in the absence of any intentional changes in dietary intake or physical activity. No significant changes in glycated hemoglobin or other lipid parameters were seen.
Strength of evidence: Evidence for weight loss is preliminary and based on small, short-duration trials, several of which lacked robust controls. No large, independent randomized controlled trials have been conducted specifically for weight management as a primary endpoint.
Preliminary animal and preclinical studies of D-tagatose showed its ability to reduce blood glucose and lipoprotein content. Compared to sucrose, D-tagatose reduces levels of total cholesterol, very low-density lipoprotein cholesterol (VLDL-C), and LDL-C in both mice and humans, and increases HDL-C.
Tagatose supplementation resulted in lowered fasting blood glucose, HbA1c, LDL, and total cholesterol in type 2 diabetes patients (Ensor et al., 2015). In another clinical trial conducted with type 2 diabetic individuals, the administration of D-tagatose (15 g three times a day) resulted in a significant reduction in HbA1c in relation to placebo, but no changes were found in triglyceride and HDL levels between groups.
Strength of evidence: Effects on LDL and total cholesterol have some human trial support. Results regarding HDL and triglycerides are inconsistent across studies. Overall, evidence for lipid effects is preliminary and mixed.
Supplementation with tagatose led to increased bacterial density and short-chain fatty acid (SCFA) production, specifically butyrate in healthy adults and propionate in adults with type 2 diabetes (Van den Abbeele et al., 2023). In vitro studies have demonstrated that tagatose as a synbiotic substrate enhances the growth of Lactobacillus casei 01 and Lactobacillus rhamnosus strain GG, reinforcing the attachment to epithelial cells, and therefore enhancing cholesterol-lowering activities.
D-tagatose, as a monosaccharide and dietary supplement, has been reported as having a wide range of applicability. In an animal study using loperamide-induced constipation in Kunming mice, the effects of D-tagatose for the prevention of constipation were evaluated; the results showed that the gastrointestinal transit rate, fecal number, and weight in six hours were significantly enhanced after administration of D-tagatose.
An ongoing clinical trial is designed to determine, in subjects with impaired fasting glucose and/or insulin resistance, if tagatose meets the definition of a prebiotic by selectively stimulating the growth of bacteria in the colon, associated with a health benefit in oral glucose tolerance, when compared to consuming a control treatment of 10 g sucrose for 4 weeks.
Strength of evidence: The fermentation of tagatose and subsequent effects have only been demonstrated in preclinical models, with limited clinical trials examining the effect of tagatose on glycemic control via the gut microbiome. Prebiotic effects in humans are promising but remain largely under-investigated in clinical settings.
In addition to being considered a non-cariogenic sugar, there is evidence in the literature that D-tagatose may have an antibacterial effect against oral species, including periodontopathogenic and cariogenic strains. Tagatose-supplemented gum may help prevent dental caries, periodontitis, and oral diseases in healthy adults (Nagamine et al., 2020).
Two studies consistently demonstrated significant reductions in colony-forming unit (CFU) counts in vitro and changes in oral bacteria in groups treated with D-tagatose alone or in mixtures compared to controls using other non-caloric sweeteners or placebos. However, the quality of the evidence was heterogeneous with certain methodological concerns. Although the findings suggest potential benefits of D-tagatose in reducing cariogenic risk, limitations such as small sample sizes and variability in study methodologies warrant caution. Further robust investigations are needed to substantiate these promising results.
Strength of evidence: The dental health claim has been recognized by the US FDA and evaluated by EFSA, but the underlying clinical trial base is small. Mechanistic in vitro evidence is stronger than clinical human evidence for this indication.
In a preclinical study, Wistar rats were allocated to experimental groups and fed control, 30% fructose-enriched, or 30% D-tagatose-enriched diets. After 24 weeks of dietary manipulation, rats underwent myocardial injury. Fructose consumption resulted in body weight increase (49%) as well as altered glucose, insulin, and lipid profiles, associated with increased I/R-induced myocardial damage, oxidative stress (36.5%), and inflammation marker expression. These findings are in agreement with previous findings showing that D-tagatose, as a carbohydrate source, did not promote obesity and hyperglycemia, and these effects were associated with lower risk of hypercholesterolemia and atherosclerosis.
Strength of evidence: Cardiovascular and antioxidant evidence for tagatose is currently limited to animal studies. No dedicated human clinical trials on cardiovascular endpoints have been published.
Research from the University of Connecticut indicates that tagatose has the potential to reduce C. difficile infection through multiple mechanisms. Its prebiotic properties appear to promote a healthier gut microbiome, while preliminary evidence suggests it may also inhibit the production of bacterial toxins. Further research is planned to investigate the specific mechanisms of action and to evaluate efficacy in clinical trials.
Strength of evidence: This application is at the preclinical/preliminary stage. No human clinical trials on this indication have been reported to date.
In the Phase 3 clinical trial for type 2 diabetes, type 2 diabetic patients not taking any blood glucose-lowering medications were administered either 15 g of D-tagatose dissolved in 125β250 mL of water three times a day or placebo with meals.
In a Phase 2 dose-ranging trial, the doses studied were 2.5 g, 5.0 g, or 7.5 g administered three times per day for six months in patients with type 2 diabetes. A Phase 2 study by Ensor et al. (2014) determined that the lowest dose of D-tagatose capable of lowering HbA1c was 5.0 g taken three times a day.
A lower dose of D-tagatose (45 g/day; 15 g three times daily) is considered to be safe in healthy human subjects because it does not show any adverse effects on plasma uric acid, glycogen levels, or liver function. Similarly, consumption of 45 g D-tagatose/day (15 g three times daily) for a period of one year does not cause any adverse effects on plasma uric acid levels in non-insulin-dependent diabetes mellitus patients.
One study investigated acute effects on blood sugar levels in 8 healthy individuals and 8 individuals with type 2 diabetes after oral intake of 75 g of D-tagatose alone and combined with 75 g of glucose. Diabetics received 75 g of D-tagatose separately at 0, 10, 15, 20, and 30 minutes before a dose of 75 g of glucose.
The EFSA has affirmed that doses of 7.5 g per meal or greater help to balance blood glucose levels.
Commercially, tagatose is available as a crystalline powder for use as a one-for-one sucrose substitute in cooking, baking, and beverages, as well as in ready-formulated dietary supplement capsules and functional food products.
D-tagatose is Generally Recognized As Safe (GRAS) by the US Food and Drug Administration (FDA). The World Health Organization's Joint Expert Committee on Food Additives (JECFA) has designated an Acceptable Daily Intake for tagatose as "ADI unspecified," which means even high intakes are not expected to have long-term toxic effects.
Gastrointestinal symptoms such as bloating, belching, flatulence, and laxation may be experienced with excessive consumption of over 30 g per serving of products containing tagatose. These symptoms are characterized as mild, transient, and not experienced by all consumers, and therefore do not pose a significant health or safety concern. In sensitive individuals, tagatose, when taken in doses higher than 10β15 grams per meal, may cause mild digestive problems such as nausea, flatulence, and diarrhea. Doses as high as 45 grams per day can be well tolerated, though.
The elevated level of plasma uric acid is associated with purine metabolism disorder and development of gout. There is a transient increase of plasma uric acid concentration in both healthy and non-insulin dependent diabetes mellitus populations following a single oral dose of 75 g of D-tagatose. Tagatose slightly increases blood uric acid levels, but there is no evidence that it increases the risk of gout. A dose of 45 g/day (15 g three times daily) is considered to be safe in healthy human subjects because it does not show any adverse effects on plasma uric acid levels.
Tagatose is probably not safe for individuals with hereditary fructose intolerance (HFI) since it is metabolized the same way as fructose, although accidental intake of small amounts of tagatose from commercial products is not likely harmful. Tagatose does not affect the absorption of fructose in individuals with fructose malabsorption, however.
Tagatose does not likely trigger an allergic reaction in individuals with milk allergy. This is because tagatose derived from dairy sources is highly purified and does not contain milk proteins.
D-tagatose may interact with some prescription drugs, especially blood sugar-lowering drugs, and could cause hypoglycemia (dangerously low blood sugar levels). In people with diabetes or a history of kidney stones, temporary rises in uric acid blood levels caused by high-dose D-tagatose may be an issue.
When tagatose consumption increases beyond 10% of the diet in animal studies, adverse effects (increased liver weight and hypertrophy) have been noticed in rats. A 5% level of tagatose is considered a safe dose without any side effects at that animal dosing level. Reproductive performance of rats is not affected even when tagatose consumption reaches up to 20 g/kg body weight per day. These findings derive from animal studies and their direct extrapolation to humans requires caution.
Health conditions that Tagatose may help support.
Body systems that Tagatose may help support.
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